302
Journal of the Royal Society of Medicine Volume 85 May 1992 associated with tumor emboli and disseminated intravascular coagulation. Arch Intern Med 1983;143:2220 Bernard CA, Sick H, Boilletot A, et aL Bone marrow necrosis. Acute microcirculation failure in myelomonocytic leukemnia. Arch Intern Med 1978;138:1567-9 Norgard MJ, Carpenter JT, Conrad ME. Bone marrow necrosis and degeneration. Arch Intern Med 1979;139:905-11 !udla V, Dusek J, Maik J, et aL Bone marrow necrosis intravitally recognized in four cases of blastic leukaemia. Folia Haemota 1990;117:799-803 Knupp Ch, Pekala PH, Cornelius P. Extensive bone marrow necrosis in patients with cancer and tumor necrosis factor activity in plasma. Am J Hemat 1988;9:215-21
References 1 Rose MA. Apparent necrosis of bone marrow in a patient with disseminated intravascular coagulation post partum. Lancet 1973;ii:730-1 2 Harigaya K, Watanabe S, Watanabe Y, et al Multiple bone marrow necrosis and disseminated intravascular coagulation. Arch Path Lab Med 1977;101:652-4 3 Ritter HL Jr, Weiden PL. Unusual association of bone marrow necrosis, disseminated intravascular coagulation and a rase 8; 16 chromosomal translocation in an adult patient with atute nonlymphocytic leukaemia. Cancer Genet Cytogenet 1987;24: 243-50 4 Ricci P, Bandini G, Baccarani M, et aL Bone marrow necrosis by diffuse metastatic intravascular obstruction. Haematologica 1982;67:754-9 5 Laso FJ, Gon7AIez-DIaz M, Paz JI, et aL Bone marrow necrosis
(Accepted 29 April 1991)
Pituitary surgery and inappropriate antidiuretic hormone secretion
tr4nssphenoidal pituitary surgery and was discharged home
J Tymms MRCP1 J D A Clark MRCP2 H B Griffith FRCS3 J P D Reckless FRCP' M Hartog FRCP2 'Department of Medicine, Royal United Hospital, Bath; 2Department of Medicine, Southmead Hospital, Bristol; and 3Department of Neurosurgery, Frenchay Hospita4 Bristol Keywords: transphenoidal surgery; inappropriate ADH secretion
Disturbance of fluid balance after pituitary surgery is well recognized and is usually due to the development of cranial diabetes insipidus (DI), which may be temporary or permanent1-. In contrast, the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) following pituitaky surgery has rarely been recorded3. Diagnosis may be difflicult as the initial symptoms are-often non.specific and aW not develop until the patient has been dischrged home. We report two patients who experienced such late manifestations of SIADH after transephenoidal operations for pituitary tumour.
Case reports Case 1 A 38-year-old man with a macroprolactinoma (plasma prolactin 78 000 mU/I) and suprasellar extension, was referred for transsphenoidal pituitary surgery. Preoperative assessment ofhis adrenal and thyroidal axes was normal. His postoperative course was uneventful, with no abnormality of fluid balance, and he was discharged home on day 5, on no medical treatment. Two days later he was readmitted with a 24-h history of lethargy and general malaise, having had three grand mal seizures on the day of admission. On examination he was drowsy, pulse rate 80/min, blood pressure 120/70, and there were no focal neurological signs. He was found to be hyponatraemic (plasma sodium 121 mmol/l) with reduced plasma osmolality (244 mosmol/kg) and hypertonic urine (640 mosmoiikg). Basal plasma cortisol, thyroid hormone levels and a short Synacthen test were normal. His fluid intake was restricted to one litre a day and, by day 3, his plasma sodium had risen to 131 mmol/l. He made a complete recovery and his plasma sodium remained normal at 139 mmol/l and 136 mmol/l, 2 weeks and 3 months, after discharge without further fluid restriction. Case 2 A 42-year-old woman with a non-functioning pituitary adenoma and normal preoperative endocrine investigations, Correwondence to: Dr J Clark, Department of Medicine, Postgrduate Centre, Southmead Hospital, Bristol BS10 5NB
6 7 8 9
except for, mild byperprolactinaemia (2000 mnU/l), underwent
after 6, days, on, no medical treatment. She was readmitted .3 days later. with lethargy, malaise and nausea and was fo4nd to be hyppnatraemw (plasma sodium 117 mmol/l), with reduced plasma osmolality (289 mosmollkg). All endocrine tests were normal. Her plasma sodium rose with fluid restriction (131 mmolll after 3 days) and was maintained after discharge, without fluid restriction (136 mmolfl after 2 months). Discussion Our two patients had clinical and endocrine findings consistei with inappropriate release of ADH, requiring their emWrgency re-admission 7 and 9 days postoperatively. Such inappropriate release- of ADI-from damaged posterior pituitary cells has been reported in the middle (remission) phase of triphasic diabetes insipidu405. However, neither patient manifested frank diabetes insipidus and so, presumably, had less than the 90% destruction oftheir supraoptic and paraventricular nuclei, which is usually associated with the development of permanent diabetes fiisipidus6. Recently increased levels of ADIH have been reported after tranasphenoidal pituitary surgery; but no association with hyponatraemia was ob4erved7. There. hag been onij one previous report of elinically significant hyponatraemia, dute to inappropriate secretion of ADH, after pituitary surgery3. Two of the three patients in this report bad no evidence of fluid disturbance intil the development of profound hyponatraemia on the 10th postoperative day, and one presented with generalized seizures. In view of the severe, and potez,tially, permanent, -neurological effects-that may res lt f1rom profound hyponatraemia, the syndrome ofinappropriate ADH secretion must be borne in mind in patients developing non-specific symptoms of weakness, lethargy and nausea shortly after discharge following pituitary surgery.
References 1 Lipsett MB, Maclean JP, West CD, Li MC, Pearson OH. An analysis of the polyuria induced by hypophysectomy in man. J Clin Endocrin Metab 1956;16:183-95 2 SeklJ, DumggD. Pavediabetsin sipidus BMJ1989;29.2-3 3 Cusick JF, Hagen TC, Findling JW. Inappropriate secretion of antidiuretic hormone after transphenoidal surgery for pituitary tumours. N Engi J Med 1984;311:36-8 4 Hollinshead WH. The interphase of diabetes insipidus. Mayo Clin Proc 1964;39:92-100 5 Laszlo FA, De Wied D. Antidiuretic hormone content of the hypothalamo-neurohypophyseal system and urinary excretion of antidiuretic hormone in rats during the development of diabetes insipidus after lesions in the pituitary stalk. J Endocrinol 1966;36:125-37 6 Daniel PM, Pritchard MML, Schurr PH. Extent of thq infarct im the anterior lobe of the human pituitary gland after stalk section. Lancet 1958i:1101-3 7 Seckl JR, Dunger DB, Bevan JS, et aL Vasopressin antagonist in early postoperative diabetes insipidus. Lancet 1990;335:1353-6 (Accepted 16 April 1991)
0141-0768/92/
,O0302-1/$02.00/0 © 1992 The Royal Society of Medicine
Journal of the Royal Society of Medicine Volume 85 May 1992 associated with tumor emboli and disseminated intravascular coagulation. Arch Intern Med 1983;143:2220 Bernard CA, Sick H, Boilletot A, et aL Bone marrow necrosis. Acute microcirculation failure in myelomonocytic leukemnia. Arch Intern Med 1978;138:1567-9 Norgard MJ, Carpenter JT, Conrad ME. Bone marrow necrosis and degeneration. Arch Intern Med 1979;139:905-11 !udla V, Dusek J, Maik J, et aL Bone marrow necrosis intravitally recognized in four cases of blastic leukaemia. Folia Haemota 1990;117:799-803 Knupp Ch, Pekala PH, Cornelius P. Extensive bone marrow necrosis in patients with cancer and tumor necrosis factor activity in plasma. Am J Hemat 1988;9:215-21
References 1 Rose MA. Apparent necrosis of bone marrow in a patient with disseminated intravascular coagulation post partum. Lancet 1973;ii:730-1 2 Harigaya K, Watanabe S, Watanabe Y, et al Multiple bone marrow necrosis and disseminated intravascular coagulation. Arch Path Lab Med 1977;101:652-4 3 Ritter HL Jr, Weiden PL. Unusual association of bone marrow necrosis, disseminated intravascular coagulation and a rase 8; 16 chromosomal translocation in an adult patient with atute nonlymphocytic leukaemia. Cancer Genet Cytogenet 1987;24: 243-50 4 Ricci P, Bandini G, Baccarani M, et aL Bone marrow necrosis by diffuse metastatic intravascular obstruction. Haematologica 1982;67:754-9 5 Laso FJ, Gon7AIez-DIaz M, Paz JI, et aL Bone marrow necrosis
(Accepted 29 April 1991)
Pituitary surgery and inappropriate antidiuretic hormone secretion
tr4nssphenoidal pituitary surgery and was discharged home
J Tymms MRCP1 J D A Clark MRCP2 H B Griffith FRCS3 J P D Reckless FRCP' M Hartog FRCP2 'Department of Medicine, Royal United Hospital, Bath; 2Department of Medicine, Southmead Hospital, Bristol; and 3Department of Neurosurgery, Frenchay Hospita4 Bristol Keywords: transphenoidal surgery; inappropriate ADH secretion
Disturbance of fluid balance after pituitary surgery is well recognized and is usually due to the development of cranial diabetes insipidus (DI), which may be temporary or permanent1-. In contrast, the syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) following pituitaky surgery has rarely been recorded3. Diagnosis may be difflicult as the initial symptoms are-often non.specific and aW not develop until the patient has been dischrged home. We report two patients who experienced such late manifestations of SIADH after transephenoidal operations for pituitary tumour.
Case reports Case 1 A 38-year-old man with a macroprolactinoma (plasma prolactin 78 000 mU/I) and suprasellar extension, was referred for transsphenoidal pituitary surgery. Preoperative assessment ofhis adrenal and thyroidal axes was normal. His postoperative course was uneventful, with no abnormality of fluid balance, and he was discharged home on day 5, on no medical treatment. Two days later he was readmitted with a 24-h history of lethargy and general malaise, having had three grand mal seizures on the day of admission. On examination he was drowsy, pulse rate 80/min, blood pressure 120/70, and there were no focal neurological signs. He was found to be hyponatraemic (plasma sodium 121 mmol/l) with reduced plasma osmolality (244 mosmol/kg) and hypertonic urine (640 mosmoiikg). Basal plasma cortisol, thyroid hormone levels and a short Synacthen test were normal. His fluid intake was restricted to one litre a day and, by day 3, his plasma sodium had risen to 131 mmol/l. He made a complete recovery and his plasma sodium remained normal at 139 mmol/l and 136 mmol/l, 2 weeks and 3 months, after discharge without further fluid restriction. Case 2 A 42-year-old woman with a non-functioning pituitary adenoma and normal preoperative endocrine investigations, Correwondence to: Dr J Clark, Department of Medicine, Postgrduate Centre, Southmead Hospital, Bristol BS10 5NB
6 7 8 9
except for, mild byperprolactinaemia (2000 mnU/l), underwent
after 6, days, on, no medical treatment. She was readmitted .3 days later. with lethargy, malaise and nausea and was fo4nd to be hyppnatraemw (plasma sodium 117 mmol/l), with reduced plasma osmolality (289 mosmollkg). All endocrine tests were normal. Her plasma sodium rose with fluid restriction (131 mmolll after 3 days) and was maintained after discharge, without fluid restriction (136 mmolfl after 2 months). Discussion Our two patients had clinical and endocrine findings consistei with inappropriate release of ADH, requiring their emWrgency re-admission 7 and 9 days postoperatively. Such inappropriate release- of ADI-from damaged posterior pituitary cells has been reported in the middle (remission) phase of triphasic diabetes insipidu405. However, neither patient manifested frank diabetes insipidus and so, presumably, had less than the 90% destruction oftheir supraoptic and paraventricular nuclei, which is usually associated with the development of permanent diabetes fiisipidus6. Recently increased levels of ADIH have been reported after tranasphenoidal pituitary surgery; but no association with hyponatraemia was ob4erved7. There. hag been onij one previous report of elinically significant hyponatraemia, dute to inappropriate secretion of ADH, after pituitary surgery3. Two of the three patients in this report bad no evidence of fluid disturbance intil the development of profound hyponatraemia on the 10th postoperative day, and one presented with generalized seizures. In view of the severe, and potez,tially, permanent, -neurological effects-that may res lt f1rom profound hyponatraemia, the syndrome ofinappropriate ADH secretion must be borne in mind in patients developing non-specific symptoms of weakness, lethargy and nausea shortly after discharge following pituitary surgery.
References 1 Lipsett MB, Maclean JP, West CD, Li MC, Pearson OH. An analysis of the polyuria induced by hypophysectomy in man. J Clin Endocrin Metab 1956;16:183-95 2 SeklJ, DumggD. Pavediabetsin sipidus BMJ1989;29.2-3 3 Cusick JF, Hagen TC, Findling JW. Inappropriate secretion of antidiuretic hormone after transphenoidal surgery for pituitary tumours. N Engi J Med 1984;311:36-8 4 Hollinshead WH. The interphase of diabetes insipidus. Mayo Clin Proc 1964;39:92-100 5 Laszlo FA, De Wied D. Antidiuretic hormone content of the hypothalamo-neurohypophyseal system and urinary excretion of antidiuretic hormone in rats during the development of diabetes insipidus after lesions in the pituitary stalk. J Endocrinol 1966;36:125-37 6 Daniel PM, Pritchard MML, Schurr PH. Extent of thq infarct im the anterior lobe of the human pituitary gland after stalk section. Lancet 1958i:1101-3 7 Seckl JR, Dunger DB, Bevan JS, et aL Vasopressin antagonist in early postoperative diabetes insipidus. Lancet 1990;335:1353-6 (Accepted 16 April 1991)
0141-0768/92/
,O0302-1/$02.00/0 © 1992 The Royal Society of Medicine
